The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Inflammatory Status Influences Aromatase and Steroid Receptor Expression in Endometriosis
Open accessAbstract
Aberrant up-regulation of aromatase in eutopic endometrium and implants from women with endometriosis has been reported. Aromatase induction may be mediated by increased cyclooxygenase-2 (COX-2). Recently, we demonstrated that progesterone receptor (PR)-A and PR-B serve an antiinflammatory role in the uterus by antagonizing nuclear factor kappaB activation and COX-2 expression. PR-C, which antagonizes PR-B, is up-regulated by inflammation. Although estrogen receptor alpha (ERalpha) is implicated in endometriosis, an antiinflammatory role of ERbeta has been suggested. We examined stage-specific expression of aromatase, COX-2, ER, and PR isoform expression in eutopic endometrium, implants, peritoneum, and endometrioma samples from endometriosis patients. Endometrial and peritoneal biopsies were obtained from unaffected women and those with fibroids. Aromatase expression in eutopic endometrium from endometriosis patients was significantly increased compared with controls. Aromatase expression in endometriosis implants was markedly increased compared with eutopic endometrium. Aromatase mRNA levels were increased significantly in red implants relative to black implants and endometrioma cyst capsule. Moreover, COX-2 expression was increased in implants and in eutopic endometrium of women with endometriosis as compared with control endometrium. As observed for aromatase mRNA, the highest levels of COX-2 mRNA were found in red implants. The ratio of ERbeta/ERalpha mRNA was significan…
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“The eutopic endometrium of women with endometriosis demonstrates significantly elevated aromatase activity compared with unaffected women (Bukulmez et al., 2008), and within affected women, aromatase expression positively predicts severity of dysmenorrhea (Maia et al., 2012).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Bukulmez et al., 2008
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Metadata
- Authors
- Bukulmez, O., Hardy, D. B., Carr, B. R., Word, R. A., & Mendelson, C. R.
- Affiliations
- Departments of Obstetrics and Gynecology (O.B., B.R.C., R.A.W., C.R.M.), The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Mendelson, Carole R.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2007-11-29
- Volume
- 149
- Issue
- 3
- Pages
- 1190-1204
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC2275353
- OpenAlex
- W2052591056
- Cited by
- 186
- References
- 0
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 4 · 2023: 9 · 2022: 4 · 2021: 9 · 2020: 8 · 2019: 10 · 2018: 12 · 2017: 11 · 2016: 10 · 2015: 11 · 2014: 15 · 2013: 10 · 2012: 12
- FWCI
- 15.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK031206, DK31206)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
- Keywords
- endometriosis, aromatase, cyclooxygenase-2, progesterone receptor isoforms, estrogen receptor alpha, estrogen receptor beta, endometrioma, eutopic endometrium, inflammation, NF-κB, disease progression
- MeSH terms
- Adult, Aromatase, Cross-Sectional Studies, Endometriosis, Endometrium, Female, Humans, Inflammation, Ovary, Peritoneum, Prospective Studies, Receptors, Estrogen, Receptors, Progesterone, RNA, Messenger, Up-Regulation, Case-Control Studies, Protein Isoforms, Estrogen Receptor alpha, Estrogen Receptor beta, Cyclooxygenase 2
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